How the study was done

The prospective study was done on 115 patients receiving treatment at the intensive care units. The study was conducted by researchers at Brigham and Women’s Hospital in Boston under the leadership of Anand Srivastava, MD, MPH. The investigators found out that of the 115 patients, the 29 who experienced AKI depicted a significant high mean plasma uric acid levels contrasted to the 86 patients who had none. The rate was 5.5 versus 4.2 mg/dl. After multivariable analysis, for every 1 mg/dl increase in uric acid at the intensive care unit admission, a 29% rise in the AKI incident was depicted. This record was shown after a number of adjustments on sex, age, APACHE II score and baseline estimated glomerular filtration rate (eGFR).

While being interviewed by Renal & Urology News, Dr Srivastava said that “Uric acid may lead to kidney injury via endothelial dysfunction, vasoconstriction, oxidative stress, and intra-tubular obstruction.”

He went on to explain that “Upon entry to the intensive care unit, higher uric acid levels are associated with an increased risk of acute kidney injury in critically ill patients. A randomized placebo-controlled trial of pharmacologic uric acid lowering should be considered to reduce the risk of acute kidney injury in critically ill patients.”

The research participants used KDIGO (Kidney Disease: Improving Global Outcomes) criteria to define the AKI incident. There wasn’t a significant difference between the patients with AKI and those without, with respect being given to age, gender composition, and race as well APACHE II score. However, the AKI sect showed less mean eGFR (76.2 vs 92.4 mL/min/1.73 m2).

Diagnosis of AKI in cancer patients

Considering that AKI incidences are determined by its definition, comparisons are most reliable if based on studies using a more or less uniform definition, as in the Risk, Injury, Failure, Loss, End stage renal disease (RIFLE), Acute Kidney Injury Network (AKIN), and Kidney Diseases Improving Global Outcomes (KDIGO) classifications.

Cancer patients mostly record a lower production of creatinine and this is followed by medications, low protein intake, inflammation, loss of cell mass and cachexia. All these have an impact of SCr independent of renal function and for that matter lower the creatinine’s sensitivity as a kidney injury marker. For that matter, a fixed level of SCr as a marker of AKI (i.e., >1.5 or 2.0 mg/dl) is inadequate as affected patients may be overlooked.